Rate of force development and torque production assessment in spastic stroke survivors

Avaliação da taxa de produção de força e torque em indivíduos com espasticidade pós-avc

Bruno Freire Caroline P Dias Lauren S Oliveira Nathália B A Goulart Fernando A Lemos Jefferson Becker Irenio Gomes Marco A Vaz About the authors

Abstract

The aim of this study was to compare the rate of force development (RFD) and maximum torque in spastic stroke survivors and healthy individuals. Fifteen stroke survivors (57.3 ± 11.2 years) with ankle spasticity and fifteen healthy individuals (59.3 ± 6.4 years) participated in this study. An isokinetic dynamometer was used to maximum voluntary isometric contraction (MVC) and RFD assessment of plantar flexors muscles of ankle, which the individuals were instructed to produce maximum torque as fast as possible. The absolute RFD was normalized by MVC (relative RFD). In results were observed significant differences in RFD of affected limb (43.3 ± 8.5 Nm/s) and unaffected limb (98.9 ± 20.4 Nm/s) compared to healthy (186.2 ± 25.2 Nm/s), but with no differences between affected and unaffected limbs (p=0.15). In relation to relative RFD, the affected limb (9.76 ± 1.1 %MVC/s) was significant different than healthy (13.08 ± 1.5 %MVC/s). The MVC produced by affected limb (46.55 ± 7.98 Nm) was significant lower than unaffected limb (84.29 ± 8.47 Nm) and, the two limbs of stroke survivors were weakness than healthy individuals (128.02 ± 9.36 Nm). Lastly, the spasticity level present higher negative correlation in relation to RFD (R= -0.725; p= 0.002) and MVC (R= -0.717; p=0.003). The spasticity promotes alterations in capacity to produce maximum force and fast force in affected and unaffected limbs of stroke survivors compared to healthy.

Key words:
Dynamometer; Muscle power; Muscle spasticity; Strength

Resumo

O objetivo desse estudo foi comparar a taxa de produção de força (TPF) e o torque máximo em indivíduos com espasticidade e saudáveis. Participaram do estudo 15 sujeitos pós-AVC (57,3 ± 11,2 anos) com espasticidade de tornozelo e 15 sujeitos saudáveis (59,0 ± 6,4 anos). Um dinamômetro isocinético foi utilizado para a avaliação da contração isométrica voluntária máxima (CVM) e da TPF dos flexores plantares do tornozelo, na qual os participantes foram instruídos a produzir força máxima o mais rápido possível. A TPF absoluta também foi normalizada pela CVM (TPF relativa). Como resultados, foram encontradas diferenças significativas na TPF absoluta do lado afetado (43,3 ± 8,5 Nm/s) e não afetado (98,9 ± 20,4 Nm/s) quando comparados com os saudáveis (186,2 ± 25,2 Nm/s), porém sem diferenças entre os membros espásticos (p=0,15). Em relação a TPF relativa, apenas o lado afetado (9,76 ± 1,1 %CVM/s) apresentou diferença em relação aos saudáveis (13,08 ± 1,5 %CVM/s). A CVM produzida pelo lado afetado (46,55 ± 7,98 Nm) foi significativamente menor quando comparado ao lado não afetado (84,29 ± 8,47 Nm) e, os dois lados foram mais fracos em comparação aos indivíduos saudáveis (128,02 ± 9,36 Nm). Por fim, o nível de espasticidade apresentou alta correlação negativa em relação a TPF (R= -0,725; p= 0,002) e a CVM (R= -0,717; p=0,003). A espasticidade gera alterações na capacidade de produzir força máxima e rápida tanto no membro afetado quanto no não afetado em indivíduos que tiveram AVC em relação a indivíduos saudáveis.

Palavras-chave:
Espasticidade muscular; Dinamometria; Força; Potência muscular

INTRODUCTION

Stroke is the main cause of acquired motor disability in adults11 WHO. The Global Burden of Disease: 2004 Update. World Health Organization, Geneva, Switzerland 2008., which begins suddenly and commonly promotes weakness and hemiparesis on the contralateral side of the body in relation to the side of the cerebral injury22 Chang SH, Francisco GE, Zhou P, Rymer WZ, Li S. Spasticity, weakness, force variability, and sustained spontaneous motor unit discharges of resting spastic-paretic biceps brachii muscles in chronic stroke. Muscle Nerve 2013;48:85-92. Among complications, damage to the upper motor neurons that in turn affect the corticospinal tract responsible for the inhibitory projection in neurons of the spinal cord motor is commonly found33 Sheean G, McGuire JR. Spastic hypertonia and movement disorders: Pathophysiology, clinical presentation, and quantification. PM R 1009;1(9):827-33.. Thus, spasticity is developed.

Spasticity is defined as the increase in tendon hyperreflexia at rest, which is the increasing myotatic reflex response coupled with increased muscle tone44 Burke D, Wissel J, Donnan GA. Pathophysiology of spasticity in stroke. Neurology 2013;80(3):20-6.. This complex motor disorder stems from a dysfunction in the central nervous system and promotes alterations at all levels of the locomotor system including muscles and joints55 Priori A, Cogiamanian F, Mrakic-Sposta S. Pathophysiology of spasticity. Neurol Sci 2006;27:307-9.. Adaptations secondary to spasticity have been observed such as increased amounts of type-I muscle fibers and muscle cell stiffness66 Lieber RL, Steinman S, Barash IA, Chambers H. Structural and functional changes in spastic skeletal muscle. Muscle Nerve 2004;29(5):615-27., smaller fascicle length and cross-sectional area77 Barber L, Barrett R, Lichtwark G. Medial gastrocnemius muscle fascicle active torque-length and Achilles tendon properties in young adults with spastic cerebral palsy. J Biomech 2012;45(15):2526-30.,88 Kwah LK, Herbert RD, Harvey LA, Diong J, Clarke JL, Martin JH, et al. Passive mechanical properties of gastrocnemius muscles of people with ankle contracture after stroke. Arch Phys Med Rehabil 2012;93(7):1185-1190. decreased muscle volume99 Barrett RS, Lichtwark GA. Gross muscle morphology and structure in spastic cerebral palsy: a systematic review. Dev Med Child Neurol 2010;52(9):794-804. and reduction in voluntary muscle activation, which compromises balance, causing deficient voluntary control1010 Foran JR, Steinman S, Barash I, Chambers HG, Lieber RL. Structural and mechanical alterations in spastic skeletal muscle. Dev Med Child Neurol 2005;47(10):713-7..

Previous studies have evaluated the ability of maximal voluntary force production in stroke survivors with spastic hemiparesis. Klein et al.1111 Klein CS, Brooks D, Richardson D, McIlroy WE, Bayley MT. Voluntary activation failure contributes more to plantar flexor weakness than antagonist coactivation and muscle atrophy in chronic stroke survivors. J Appl Physiol 2010;109(5):1337-46. observed decreased plantar flexor strength of approximately 60% in ankle joint on the affected limb compared to the unaffected limb, and McCrea et al.1212 McCrea PH, Eng JJ, Hodgson AJ. Time and magnitude of torque generation is impaired in both arms following stroke. Muscle Nerve 2003;28:46-53. observed an average reduction of 53% in isometric torque on the affected arm compared to the unaffected arm. There are several causes that can be indicated as responsible for strength deficit secondary to spasticity such as muscle atrophy, decreased number of motor units, alterations on muscle recruitment order, decreased firing rate and muscle activation capacity1313 Eng JJ, Kim CM, Macintyre DL. Reliability of lower extremity strength measures in persons with chronic stroke. Arch Phys Med Rehabil 2002;83:322-8.,1414 Arene N, Hidler J. Understanding motor impairment in the paretic lower limb after a stroke: a review of the literature. Top Stroke Rehabil 2009;16(5):346-6..

A parameter related to force production capacity and important for the functional evaluation of fast muscle contraction is the rate of force development (RFD). This index has been the most widely used to represent the explosive force and is obtained by the force-time variation ratio, which is also an important neuromuscular performance parameter1515 Corvino RB, Caputo F, Oliveira AC, Greco CC, Denadai BS. Taxa de desenvolvimento de força em diferentes velocidades de contrações musculares. Rev Bras Med Esporte 2009;15(6):428-31.. RFD is relevant precisely because, according to Suetta et al.1616 Suetta C, Aagaard P, Rosted A, Jakobsen AK, Duus B, Kjaer M, et al. Training-induced changes in muscle CSA, muscle strength, EMG, and rate of force development in elderly subjects after long-term unilateral disuse. J Appl Physiol 2004;97(5):1954-61., the ability of individuals to produce fast force is related with daily activities such as walking, climbing and going down stairs. Also, the increase in RFD reflects higher level of muscle strength in the initial muscle contraction phase1717 Aagard P, Simonsen EB, Andersen JL, Magnusson P, Dyhre-Poulsen P. Increased rate of force development and neural drive of human skeletal muscle following resistance training. J Appl Physiol 2002;93:1318-1326. which enables a fast response in balance disturbance situations, preventing falls. Considering the alterations in motor control promoted by spasticity and on muscles in spastic individuals, it is important to study RFD and the maximal force production in this population. However, few studies have assessed these variables in stroke survivors with spasticity.

Thus, the aim of this study was to compare the rate of force development (RFD) and maximum torque production of plantar flexors between stroke survivors with spasticity and healthy subjects and correlate the spasticity level with the variables investigated.

METHODS

Fifteen stroke survivors with ankle spasticity participated in this study. The spasticity level was assessed by the Modified Ashworth scale. Inclusion criteria were: (1) presence of hemiparesis spasticity for at least one year; (2) being able to walk without any assistance; (3) no history of orthopaedic surgery in any lower limb; (4) no use of medication to treat spasticity or use of ortheses; (5) cognitive capacity to perform assessments; (6) being able to remain seated for at least one hour. Fifteen healthy and sedentary individuals with no neurological or muscle disorder and with similar age participated in the control group. All subjects signed an informed consent form to participate in the study and the experimental protocol was approved by the Ethics Committee in Human Research of the institution where the study was conducted (Protocol number 18440 UFRGS and Protocol number 10-5179 PUCRS).

Experimental design

The experiment consisted of two sessions with interval of one week between them for all participants. Each limb was tested in one session using the same protocol. Only the dominant leg of healthy subjects was considered for analysis and used as healthy limb.

Evaluation procedures

An isokinetic dynamometer (Biodex Medical System, Shirley - NY, USA) was used for the positioning of the ankle joint and assessment of RFD and torque production. Participants were seated on the dynamometer chair and positioned with trunk and hips fixed by adjustable straps, with knee fully extended and ankle at 0° (foot perpendicular to leg). The ankle joint rotation axis (defined by the center of the medial/lateral malleolus) was aligned with the dynamometer axis to minimize rotations out of the intended motion plane.

Subsequently, participants performed three maximal voluntary isometric contractions (MVC) of plantar flexion at 0° for 5 seconds. Participants were oriented to exert maximal force as fast as possible and maintain this effort for at least one second. The maximum active torque recorded among the three contractions was used for further analysis. Before data acquisition protocols, all participants performed three submaximal voluntary isometric contractions of plantar flexion as familiarization protocol, and a 2-min resting time was respected between contractions (familiarization and evaluation) to avoid potential fatigue effects in torque production.

Absolute RFD was defined as the slope of the torque-time curve (∆moment/∆time) in incrementing time period of 0-250 ms from the onset of maximal isometric contraction. A routine in MATLAB software (MATLAB version 7.3.0.267, MathWorks, Inc., Natick, MA) was used to obtain torque and RFD variables during CVM. Also, the relative RFD that was obtained with the absolute RFD normalized by MVC (RFD/MVC, present in %MVC/s) was measured at same time period.

Data analysis

Data homogeneity was tested using Levene's test and distribution normality was tested and confirmed by the Shapiro-Wilk test. For unpaired samples, the student t test was used to compare age and anthropometric variables between groups. One-way ANOVA was used to determine the existence of significant differences in RFD and torque between limbs. Correlation test was performed by the Pearson test. Statistical analysis was performed using SPSS software version 17.0 with significance level of α = 0.05.

RESULTS

There were no significant differences for age, body mass and height (p=0.60, p=0.65 and p=0.46, respectively) between groups (stroke vs. healthy). Anthropometric and clinical variables are shown in table 1.

Table 1
Characteristics of participants (mean ± SD).

The affected limb showed significantly lower torque production compared with the unaffected limb (46.55 ± 7.98 Nm and 84.29 ± 8.47 Nm, respectively; p≤0.001). Healthy individuals (128.02 ± 9.36 Nm) were stronger in maximum isometric torque production than the affected (p≤0.001) and unaffected limb (p≤0.001) of stroke survivors. MVC results are shown in figure 1.

Figure 1
Maximum voluntary isometric contraction (MVC) of plantar flexors in affected and unaffected limbs of stroke survivors and dominant limb of healthy subjects. *Difference to healthy limb;

In relation to absolute RFD, affected limb (43.3 ± 8.5 Nm/s) and unaffected limb (98.9 ± 20.4 Nm/s) showed significant lower values (p≤0.01 and p=0.04, respectively) compared to healthy limb (186.2 ± 25.2 Nm/s). On the other hand, there were no significant differences (p=0.15) between affected and unaffected limbs of stroke survivors. Results are shown in figure 2.

Figure 2
Absolute rate of force development (RFD) of plantar flexors in affected and unaffected limbs of stroke survivors and dominant limb of healthy subjects. *Difference to healthy limb; Data expressed as mean ± ED. p<0.05.

When normalized by MVC (relative RFD), affected limb (9.76 ± 1.1 %MVC/s) was significant lower compared to healthy individuals (13.08 ± 1.5 %MVC/s). There were no significant differences between unaffected limb (10.87 ± 1.4 %MVC/s) and healthy limb. Results of relative RFD are shown in figure 3.

Figure 3
Relative rate of force development (RFD) of plantar flexors in affected and unaffected limbs of stroke survivors and dominant limb of healthy subjects. *Difference to healthy limb; Data expressed as mean ± ED. p<0.05.

High negative correlation (R= -0.717; p=0.003) between MVC and spasticity level (ASW scale) and high negative correlation (R= -0.725; p= 0.002) between RFD and spasticity level were observed.

DISCUSSION

The aim of this study was to investigate possible changes in muscle force production capacity and ankle joint power in order to identify functional impairment secondary to spasticity compared to healthy subjects. The findings demonstrate reduction in RFD and maximum force production of ankle muscles in spastic individuals but with no significant difference of muscle power between limbs of stroke survivors, which identify functional changes in both affected and unaffected limbs in relation to healthy subjects.

In this context, results of previous studies have shown decreased RDF of 64%1818 Tammik K, Matlep M, Ereline J, Gapeyeva H, Pääsuke M. Quadriceps femoris muscle voluntary force and relaxation capacity in children with spastic diplegic cerebral palsy. Pediatr Exerc Sci 2008;20:18-28. and 70%1919 Moreau NG, Falvo M, Damiano DL. Rapid Force Generation is Impaired in Cerebral Palsy and is Related to Decreased Muscle Size and Functional Mobility. Gait Posture 2012;35(1):154-8. in spastic children compared to children with typical development, suggesting loss of muscle efficiency caused by spasticity. The decrease in RFD observed in affected and unaffected limbs demonstrated the lower speed with which maximum force can be generated by plantiflexor muscles; however, this difference was not observed between affected and unaffected limbs. Dissimilarly, Fimland et al.2020 Fimland MS, Moen PMR, Hill T, Gjellesvik TI, Tørhaug T, Helgerud J, et al. Neuromuscular performance of paretic versus non-paretic plantar flexors after stroke. Eur J Appl Physiol 2011;111(12):3041-9. found reduction in RFD of affected limbs compared to unaffected limbs in stroke survivors. The authors found reductions ranging from 54% to 67% between limbs and justify the findings due to low neuromuscular activity and atrophy promoted by the commitment time of 6.5 (0.8 to 20.9) years of stroke, on average. However, the present study showed longer stroke commitment time (7.4 ± 5.8 years), but the stroke commitment time may not be the proper justification. A previous study2020 Fimland MS, Moen PMR, Hill T, Gjellesvik TI, Tørhaug T, Helgerud J, et al. Neuromuscular performance of paretic versus non-paretic plantar flexors after stroke. Eur J Appl Physiol 2011;111(12):3041-9.also showed results of maximum contraction of plantiflexor muscles not normalized by the mass of each individual, which may have been responsible for differences among findings in these studies. In the same way, the spasticity level of participants evaluated by Fimland et al.2020 Fimland MS, Moen PMR, Hill T, Gjellesvik TI, Tørhaug T, Helgerud J, et al. Neuromuscular performance of paretic versus non-paretic plantar flexors after stroke. Eur J Appl Physiol 2011;111(12):3041-9. was not described, thus the difference in RFD can have other reasons.

The fact that the unaffected limb had lower absolute RFD compared to healthy subjects can be justified by functional and morphological differences caused by spasticity. Malaya et al.2121 Malaiya R, McNee AE, Fry NR, Eve LC, Gough M, Shortland AP. The morphology of the medial gastrocnemius in typically developing children and children with spastic hemiplegic cerebral palsy. J Electromyogr Kinesiol 2007;17(6):657-63. observed lower medial gastrocnemius muscle length in the unaffected limb of hemiplegic cerebral palsy children (0.165 ± 0.028 m) compared to children with typical development (0.191 ± 0.035 m). The authors could not explain the results, but the present study reported reduction in RFD and in maximum force production, demonstrating the inability acquired by the unaffected limb in relation to healthy subjects, which could be a result of morphological or functional adaptation. While the unaffected limb can take higher level of daily activity resulting from increased functional dependence, spasticity leads patients to reduce their overall mobility, which results in decreased functional capacity of apparently healthy muscle 22. In this context, further studies should be carried out in order to assess the relationship of the unaffected side with spasticity and possible adaptations.

RFD is an aspect influenced by several factors, among which fiber muscle length and thickness, fiber type and composition1717 Aagard P, Simonsen EB, Andersen JL, Magnusson P, Dyhre-Poulsen P. Increased rate of force development and neural drive of human skeletal muscle following resistance training. J Appl Physiol 2002;93:1318-1326.,1919 Moreau NG, Falvo M, Damiano DL. Rapid Force Generation is Impaired in Cerebral Palsy and is Related to Decreased Muscle Size and Functional Mobility. Gait Posture 2012;35(1):154-8., which are features that can be modified by spasticity. Kwah et al.88 Kwah LK, Herbert RD, Harvey LA, Diong J, Clarke JL, Martin JH, et al. Passive mechanical properties of gastrocnemius muscles of people with ankle contracture after stroke. Arch Phys Med Rehabil 2012;93(7):1185-1190. assessed spastic stroke survivors using ultrasound and observed lower length of gastrocnemius medialis (436 mm) and fascicle muscles (44 mm) compared to healthy subjects (444 and 50 mm, respectively). Other studies have also shown lower length of fascicle muscles in hemiplegic spastic individuals2323 Li L, Tong KY, Hu X. The effect of poststroke impairments on brachialis muscle architecture as measured by ultrasound. Arch Phys Med Rehabil 2007;88:243-50.,2424 Gao F, Grant TH, Roth EJ, Zhang L. Changes in passive mechanical properties of the gastrocnemius muscle at the muscle fascicle and joint levels in stroke survivors . Arch Phys Med Rehabil 2009;90(5):819-26.. All authors related the lower length of fascicle muscles with increasing stiffness in muscle tissue due to shortened position of the joint and with muscle spasticity88 Kwah LK, Herbert RD, Harvey LA, Diong J, Clarke JL, Martin JH, et al. Passive mechanical properties of gastrocnemius muscles of people with ankle contracture after stroke. Arch Phys Med Rehabil 2012;93(7):1185-1190.,2424 Gao F, Grant TH, Roth EJ, Zhang L. Changes in passive mechanical properties of the gastrocnemius muscle at the muscle fascicle and joint levels in stroke survivors . Arch Phys Med Rehabil 2009;90(5):819-26.., Friden and Lieber2525 Friden J, Lieber RL. Spastic muscle cells are shorter and stiffer than normal cells. Muscle Nerve 2003;27:157-64. had previously found lower lengths of spastic fascicle muscles in vitro, while Svantensson et al.2626 Svantesson U, Takahashi H, Carlsson U, Danielsson A, Sunnerhagen KS. Muscle and tendon stiffness in patients with upper motor neuron lesion following a stroke. Eur J Appl Physiol 2000;82(4):275-9. observed increased muscle stiffness in the affected limb compared to the unaffected limb in stroke survivors. The ratio between fascicle length and RFD occurs through an increase in number of sarcomeres in series, indicated by fascicle length results in an increase of fiber shortening velocity, and consequently increase of RFD1919 Moreau NG, Falvo M, Damiano DL. Rapid Force Generation is Impaired in Cerebral Palsy and is Related to Decreased Muscle Size and Functional Mobility. Gait Posture 2012;35(1):154-8.. In addition, the concentration and type of fiber can be altered, histopathological studies found atrophy of type-2 muscle fibers in spastic stroke individuals2727 Hachisuka K, Umezu Y, Ogata H. Disuse muscle atrophy of lower limbs in hemiplegic patients. Arch Phys Med Rehabil 1997;78(1):13-8.. This type of fiber is responsible for fast contraction, which can modify RDF.

Maximum torque is representative of the maximum capacity of an individual to generate force, and is associated with intrinsic muscle ability and muscle activation capacity2828 Dalton BH, Harwood B, Davidson AW, Rice CL. Triceps surae contractile properties and firing rates in the soleus of young and old men. J Appl Physiol 2009;107:1781-8.. The results of this study corroborate those obtained by Klein et al.1111 Klein CS, Brooks D, Richardson D, McIlroy WE, Bayley MT. Voluntary activation failure contributes more to plantar flexor weakness than antagonist coactivation and muscle atrophy in chronic stroke survivors. J Appl Physiol 2010;109(5):1337-46., who found lower torque values, by about one third, in plantarflexor muscles of the affected limb (56.7 ± 57.4 Nm) compared to unaffected limb (147 ± 35.7 Nm) in stroke survivors. Additionally, studies justify that neuromuscular weakness is a common finding in the affected limb of spastic hemiplegic individuals2020 Fimland MS, Moen PMR, Hill T, Gjellesvik TI, Tørhaug T, Helgerud J, et al. Neuromuscular performance of paretic versus non-paretic plantar flexors after stroke. Eur J Appl Physiol 2011;111(12):3041-9.,2929 Horstman A, Gerrits K, Beltman M, Janssen T, Konijnenbelt M, de Haan A. Muscle function of knee extensors and flexors after stroke is selectively impaired at shorter muscle lengths. J Rehabil Med 2009;41:317-21. and unaffected limb in relation to healthy subjects 2222 Chou LW, Palmer JA, Binder-Macleod S, Knight CA. Motor unit rate coding is severely impaired during forceful and fast muscular contractions in individuals post stroke. J Neurophysiol 2013;109(12):2947-54.,3030 Elder GC, Kirk J, Stewart G, Cook K, Weir D, Marshall A, Leahey L. Contributing factors to muscle weakness in children with cerebral palsy. Dev Med Child Neurol 2003;45(8):542-50., therefore, a decrease in force production resulting from spasticity was expected. Furthermore, maximum force production appears to be an important aspect in muscle power, since when RFD was normalized by MVC (relative RFD), the difference between affected and healthy limb was not statistically significant. Fimland et al.2020 Fimland MS, Moen PMR, Hill T, Gjellesvik TI, Tørhaug T, Helgerud J, et al. Neuromuscular performance of paretic versus non-paretic plantar flexors after stroke. Eur J Appl Physiol 2011;111(12):3041-9. explain that there can be no difference in the neuromuscular recruitment capacity between limbs, but morphological alterations such as muscle atrophy explain the difference observed in absolute and not in relative RFD on unaffected limb compared to healthy subjects.

The high negative correlation between spasticity level with RFD and maximum torque suggests the functional impairment of spastic individuals. The adaptations in reflex sensibility to which spinal motor neurons increase the muscle activation2222 Chou LW, Palmer JA, Binder-Macleod S, Knight CA. Motor unit rate coding is severely impaired during forceful and fast muscular contractions in individuals post stroke. J Neurophysiol 2013;109(12):2947-54. associated with interrupt motor stimulation from the supraspinal centers developed by spasticity results in impairment of force modulation and production1414 Arene N, Hidler J. Understanding motor impairment in the paretic lower limb after a stroke: a review of the literature. Top Stroke Rehabil 2009;16(5):346-6.. Thus, the ability to produce maximum force and/or muscle power is severely impaired by spasticity.

It is noteworthy that there are some limitations to consider in the findings of this study. Neuromuscular impairment due to spasticity is not restricted to proper muscle contraction but also to the sensory system, which participants reported loss of sensation and proprioception in the affected limb. The position on the dynamometer can have enhanced this limitation with the stretching of the posterior leg muscle. In addition, the level of muscle activation through electromyography (EMG) was not measured. It is suggested the use of EMG to analyze the alterations in motor recruitment and muscle activation.

CONCLUSION

Spasticity promotes adaptations in muscle functional capacity, reducing its performance through the decreased rate of force development and maximum force production, affecting both affected and unaffected limbs. The high negative correlation between the rate of force development and maximum force production with spasticity level suggests that spastic muscles without appropriate intervention can become increasingly less functional.

REFERENCES

  • 1
    WHO. The Global Burden of Disease: 2004 Update. World Health Organization, Geneva, Switzerland 2008.
  • 2
    Chang SH, Francisco GE, Zhou P, Rymer WZ, Li S. Spasticity, weakness, force variability, and sustained spontaneous motor unit discharges of resting spastic-paretic biceps brachii muscles in chronic stroke. Muscle Nerve 2013;48:85-92
  • 3
    Sheean G, McGuire JR. Spastic hypertonia and movement disorders: Pathophysiology, clinical presentation, and quantification. PM R 1009;1(9):827-33.
  • 4
    Burke D, Wissel J, Donnan GA. Pathophysiology of spasticity in stroke. Neurology 2013;80(3):20-6.
  • 5
    Priori A, Cogiamanian F, Mrakic-Sposta S. Pathophysiology of spasticity. Neurol Sci 2006;27:307-9.
  • 6
    Lieber RL, Steinman S, Barash IA, Chambers H. Structural and functional changes in spastic skeletal muscle. Muscle Nerve 2004;29(5):615-27.
  • 7
    Barber L, Barrett R, Lichtwark G. Medial gastrocnemius muscle fascicle active torque-length and Achilles tendon properties in young adults with spastic cerebral palsy. J Biomech 2012;45(15):2526-30.
  • 8
    Kwah LK, Herbert RD, Harvey LA, Diong J, Clarke JL, Martin JH, et al. Passive mechanical properties of gastrocnemius muscles of people with ankle contracture after stroke. Arch Phys Med Rehabil 2012;93(7):1185-1190.
  • 9
    Barrett RS, Lichtwark GA. Gross muscle morphology and structure in spastic cerebral palsy: a systematic review. Dev Med Child Neurol 2010;52(9):794-804.
  • 10
    Foran JR, Steinman S, Barash I, Chambers HG, Lieber RL. Structural and mechanical alterations in spastic skeletal muscle. Dev Med Child Neurol 2005;47(10):713-7.
  • 11
    Klein CS, Brooks D, Richardson D, McIlroy WE, Bayley MT. Voluntary activation failure contributes more to plantar flexor weakness than antagonist coactivation and muscle atrophy in chronic stroke survivors. J Appl Physiol 2010;109(5):1337-46.
  • 12
    McCrea PH, Eng JJ, Hodgson AJ. Time and magnitude of torque generation is impaired in both arms following stroke. Muscle Nerve 2003;28:46-53.
  • 13
    Eng JJ, Kim CM, Macintyre DL. Reliability of lower extremity strength measures in persons with chronic stroke. Arch Phys Med Rehabil 2002;83:322-8.
  • 14
    Arene N, Hidler J. Understanding motor impairment in the paretic lower limb after a stroke: a review of the literature. Top Stroke Rehabil 2009;16(5):346-6.
  • 15
    Corvino RB, Caputo F, Oliveira AC, Greco CC, Denadai BS. Taxa de desenvolvimento de força em diferentes velocidades de contrações musculares. Rev Bras Med Esporte 2009;15(6):428-31.
  • 16
    Suetta C, Aagaard P, Rosted A, Jakobsen AK, Duus B, Kjaer M, et al. Training-induced changes in muscle CSA, muscle strength, EMG, and rate of force development in elderly subjects after long-term unilateral disuse. J Appl Physiol 2004;97(5):1954-61.
  • 17
    Aagard P, Simonsen EB, Andersen JL, Magnusson P, Dyhre-Poulsen P. Increased rate of force development and neural drive of human skeletal muscle following resistance training. J Appl Physiol 2002;93:1318-1326.
  • 18
    Tammik K, Matlep M, Ereline J, Gapeyeva H, Pääsuke M. Quadriceps femoris muscle voluntary force and relaxation capacity in children with spastic diplegic cerebral palsy. Pediatr Exerc Sci 2008;20:18-28.
  • 19
    Moreau NG, Falvo M, Damiano DL. Rapid Force Generation is Impaired in Cerebral Palsy and is Related to Decreased Muscle Size and Functional Mobility. Gait Posture 2012;35(1):154-8.
  • 20
    Fimland MS, Moen PMR, Hill T, Gjellesvik TI, Tørhaug T, Helgerud J, et al. Neuromuscular performance of paretic versus non-paretic plantar flexors after stroke. Eur J Appl Physiol 2011;111(12):3041-9.
  • 21
    Malaiya R, McNee AE, Fry NR, Eve LC, Gough M, Shortland AP. The morphology of the medial gastrocnemius in typically developing children and children with spastic hemiplegic cerebral palsy. J Electromyogr Kinesiol 2007;17(6):657-63.
  • 22
    Chou LW, Palmer JA, Binder-Macleod S, Knight CA. Motor unit rate coding is severely impaired during forceful and fast muscular contractions in individuals post stroke. J Neurophysiol 2013;109(12):2947-54.
  • 23
    Li L, Tong KY, Hu X. The effect of poststroke impairments on brachialis muscle architecture as measured by ultrasound. Arch Phys Med Rehabil 2007;88:243-50.
  • 24
    Gao F, Grant TH, Roth EJ, Zhang L. Changes in passive mechanical properties of the gastrocnemius muscle at the muscle fascicle and joint levels in stroke survivors . Arch Phys Med Rehabil 2009;90(5):819-26.
  • 25
    Friden J, Lieber RL. Spastic muscle cells are shorter and stiffer than normal cells. Muscle Nerve 2003;27:157-64.
  • 26
    Svantesson U, Takahashi H, Carlsson U, Danielsson A, Sunnerhagen KS. Muscle and tendon stiffness in patients with upper motor neuron lesion following a stroke. Eur J Appl Physiol 2000;82(4):275-9.
  • 27
    Hachisuka K, Umezu Y, Ogata H. Disuse muscle atrophy of lower limbs in hemiplegic patients. Arch Phys Med Rehabil 1997;78(1):13-8.
  • 28
    Dalton BH, Harwood B, Davidson AW, Rice CL. Triceps surae contractile properties and firing rates in the soleus of young and old men. J Appl Physiol 2009;107:1781-8.
  • 29
    Horstman A, Gerrits K, Beltman M, Janssen T, Konijnenbelt M, de Haan A. Muscle function of knee extensors and flexors after stroke is selectively impaired at shorter muscle lengths. J Rehabil Med 2009;41:317-21.
  • 30
    Elder GC, Kirk J, Stewart G, Cook K, Weir D, Marshall A, Leahey L. Contributing factors to muscle weakness in children with cerebral palsy. Dev Med Child Neurol 2003;45(8):542-50.

Publication Dates

  • Publication in this collection
    May-Jun 2015

History

  • Received
    15 Jan 2015
  • Accepted
    11 Mar 2015
Universidade Federal de Santa Catarina Universidade Federal de Santa Catarina, Campus Universitário Trindade, Centro de Desportos - RBCDH, Zip postal: 88040-900 - Florianópolis, SC. Brasil, Fone/fax : (55 48) 3721-8562/(55 48) 3721-6348 - Florianópolis - SC - Brazil
E-mail: rbcdh@contato.ufsc.br